Cancer is, at its heart, a disease of uncontrolled cell growth. There are many pathways that control cell growth and senescence, so it is not surprising that in cancer mutations are found in several different genes associated with cell growth and senescence. The most common mutations found in humans are mutations in the gene for a protein called p53. p53 activates cell suicide or permanent growth arrest in stressed cells or cells with DNA damage. The mutations in cancer cells inactivate p53, preventing it from stopping out of control cells.

If Wells is right, and mutations are not responsible for (or central to) tumourogenesis, then inactivation or deletion of p53 should do very little. In fact, p53 is shown to be a key player in experimental models. In tissue culture, deletion of p53 alone can send cells into uncontrolled growth. In mice that have had p53 knocked out, virtually all of them develop tumours, while the control mice had no tumours[5]. This strongly suggests that mutations of p53 play a major role in generating tumours. All this was known when Wells wrote his TOPS article, but he mentions none of this evidence.

Three recent papers take the p53 a step further [1,2,3]. In these papers, p53 is replaced or reactivated in tumours in mice. If Wells is right, then reactivating p53 should be of little effect. The three recent papers used different techniques to reactivate p53. Despite this, and the different tumour types in the three papers, reactivation of p53 expression led universally to a prompt and impressive regression of the tumours in vivo. These results reinforce the role of mutations in p53 in cancer.

Wells's favoured explanation for tumourogenseis is that chromosomal abnormalities, generated by centrosomes, are the key to cancer. I have dealt with his model of centrosomes before, but I will remind people that while chromosomal abnormalities are seen in many cancers, they are not seen in all cancers. Another recent paper has shown that in animals genetically engineered to have increased levels of chromosomal abnormalities [4], chemically or genetically induced tumour formation was inhibited. Thus, in certain kinds of cancer, chromosomal instability prevents tumourogenesis, the exact opposite of what Wells predicted.

Once again, real research trumps the tales of evolution deniers spun from airy nothingness. Is it any wonder that they do not expose their ideas to peer-review?